Cordy, Boney, and Others | Arthritis Information

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I friends mom is currently undergoing IV immunoglobulin therapy for her out of control Lupus. It is also used to treat intractable RA. Have you read on this...or looked into this therapy? I have not seem much on this subject posted here and was hoping for some feedback. A friend's son had it for Kawasaki's (I think it is the only treatment for that?).  He was in the hospital a few days, but did fine with it and it worked for him.  I hope your friend's mom has success, too. hi lorster i have not heard of this for ra my son had kawasaki and as
susan said IV immunoglobulin is given..not sure if kawasaki can return..

IVIG is given as a plasma protein replacement therapy (IgG) for immune deficient patients which have decreased or abolished antibody production capabilities. In these immune deficient patients, IVIG is administered to maintain adequate antibodies levels to prevent infections and confers a passive immunity. Treatment is given every 3-4 weeks. In the case of patients with autoimmune disease, IVIg is administered at a high dose (generally 1-2 grams IVIG per kg body weight) to attempt to decrease the severity of the autoimmune disease.

The precise mechanism by which IVIG suppresses harmful inflammation has not been definitively established but is believed to involve the inhibitory Fc receptor.[1][2] The actual primary target(s) of IVIG in autoimmune disease are still unclear, however. IVIG may work via a multi-step model where the injected IVIG first forms a type of immune complex in the patient. [3] Once these immune complexes are formed, they interact with activating Fc receptors on dendritic cells[4]which then mediate anti-inflammatory effects helping to reduce the severity of the autoimmune disease or inflammatory state.

Additionally, the donor antibody may bind directly with the abnormal host antibody, stimulating its removal. Alternatively, the massive quantity of antibody may stimulate the host's complement system, leading to enhanced removal of all antibodies, including the harmful ones. IVIG also blocks the antibody receptors on immune cells (macrophages), leading to decreased damage by these cells, or regulation of macrophage phagocytosis.

IVIG may also regulate the immune response by reacting with a number of membrane receptors on T cells, B cells, and monocytes that are pertinent to autoreactivity and induction of tolerance to self.[5]

A recent report stated that IVIG application to activated T cells leads to their decreased ability to engage microglia. As a result of IVIG treatment of T cells, the findings showed reduced levels of tumor necrosis factor-alpha and interleukin-10 in T cell-microglia co-culture. The results add to the understanding of how IVIG may affect inflammation of the central nervous system in autoimmune inflammatory diseases.[6]

IVIG is useful in some acute infection cases such as in Kawasaki's Disease and pediatric HIV infection.




a bit more info

Acute myocardial infarction associated with high dose intravenous immunoglobulin infusion for autoimmune disorders: a study of four cases

Abstract:

Intravenous immunoglobulin infusions should be used with caution in people with autoimmune disorders who also have risk factors for heart disease. The case reports of four patients who had a heart attack while receiving intravenous immunoglobulin are discussed.


a little more .... where is lynn49  phewwww

Objective. To report the short and longterm effect of intravenous immunoglobulin (IVIG) in patients with systemic onset juvenile rheumatoid arthritis (SOJRA). Methods. A retrospective chart review of 27 patients with SOJRA treated with IVIG and followed for 37.1 ± 18.2 months was undertaken. Indications for treatment were fever, arthritis, or steroid dependency. Results. We treated 27 patients with SOJRA with IVIG monthly for 3-54 months. Six months after IVIG therapy, 20 patients had at least a 50% decrease in at least one of the following : the number of days of fever ; prednisone dose ; or the number of active joints. Five patients failed to respond to IVIG, and 2 dropped out after 3 and 4 months. At last followup visit (mean 37.6 ± 18 months), 11 of the initial 20 responder group patients were in remission, while 3 had significantly improved but still had active arthritis, and 6 were now unresponsive. Of the initial 5 patients in the nonresponder group, 4 had nonresponsive arthritis and 1 had improved at last followup. Three patients in the responder group subsequently developed other diseases. Conclusion. The main benefit of IVIG therapy to most of our patients was a significant improvement in the systemic features, with resolution of fever and a significant reduction in the steroid dose. The efficacy of IVIG in altering the course of arthritis was less predictable. We suggest that IVIG has a role in the management of SOJRA, but it should be limited to patients with severe SOJRA in whom prolonged unresponsiveness to standard therapy is present.



and 1 more which i thought interesting about the immunoglobulin in ra

summary  Immunoglobulins are often high in active rheumatoid arthritis and fall when treatment with a slow-acting anti-rheumatic drug is instituted. We assessed the value of monitoring immunoglobulins during penicillamine therapy; 145 patients were followed for up to 5 years, IgA, IgM and IgG levels were compared to 12 other clinical and laboratory variables on 903 occasions. Mean levels of IgA and IgG fell by 10–30%. These changes were less than with ESR or clinical measures such as articular index and duration of morning stiffness. Immunoglobulin levels showed weak correlations with other variables. Only a small number of patients had hypogammuglobulineamia. Initially, 5 cases had low IgA with subsequent falls in 3 more. Initially, 2 cases had low IgG with subsequent falls in 5 more. No patients had low IgM levels. These changes seemed clinically irrelevant. Radiological progression was related to IgA levels. Patients with persistently high rates of radiological progression had persistently higher serum IgA. We conclude that IgM gives the most pattern of response. IgA gives more theoretically interesting information, especially concerning radiological progression. There is only a limited amount of clinically valuable information gained from measuring immunoglobulins.


found this interesting about adalimumbab...\ humira  /

Tumor necrosis factor (TNF) is a proinflammatory cytokine that is involved with normal inflammatory and immune responses and with the pathogenesis of chronic inflammatory medical conditions, such as rheumatoid arthritis, psoriatic arthritis, plaque psoriasis, and Crohn's disease. The newest therapies for these inflammatory conditions include the TNF biologic response modifiers infliximab, etanercept, and adalimumab. Adalimumab is a human recombinant immunoglobulin G1 anti-TNF monoclonal antibody. As monotherapy, or in combination with methotrexate or other traditional disease-modifying antirheumatic drugs, adalimumab can produce improvements in the signs and symptoms associated with rheumatoid arthritis and can slow progression of the joint destruction. The adverse effect profile of adalimumab seems to be comparable to that of etanercept. Adalimumab also seems to be useful in the treatment of psoriasis, psoriatic arthritis, and Crohn's disease; however, none of these indications are approved by the US Food and Drug Administration, and the optimal dosing regimen for these indications has not been established.

PMID: 15580154 [PubMed - indexed for MEDLINE]



Boney, do you have some heart problems that may make you ineligible for a treatment like this? I know I have given this therapy although, I cannot remember all the reasons, I don't recall any initial bad effects. Check this out. Maybe this is something that may show some promise for you and others. I know it is a blood product and that needs to be taken into consideration.hi lorster i found this very intersting . especially as i only have pred
to use.. my doc wanted me on 20mg 1 day and 10 mg the other 6 days
i found 12.5mg daily best.. allthough not high doses.. being a long term
user any reduction is good.. i have high blood pressure now. and take
ramipril i see my rheumatologist next month i will ask him about this..
i do know somebody whith lupus but is being controlled by
azorthiaprin and low dose pred.. i hope the treatment works for
your freinds mum..
Boney

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